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EEG Neurofeedback for Treating Psychiatric Disorders: Page 2 of 3

EEG Neurofeedback for Treating Psychiatric Disorders: Page 2 of 3

Additional research suggests that EEG neurofeedback may be an effective alternative to psychostimulants in the treatment of ADHD if medication is ineffective or has adverse effects or if patients are noncompliant (Rossiter and La Vaque, 1995). In one case study, a 36-year-old female diagnosed with ADHD, temporal seizure disorder and borderline personality disorder received 30 weekly sessions of SMR neurofeedback training and carbamazepine (Tegretol) (Hansen et al., 1996). The patient initially was reluctant to take carbamazepine but became compliant after starting neurofeedback training. However, because of the drug's side effects, she stopped, restarted and then again discontinued her medication. Following 17 sessions of neurofeedback, her quantitative EEG (QEEG) showed relative powers within normal ranges. Carbamazepine increased the favorable effect of neurofeedback on TOVA performance in the early phase of treatment. Although the subject's TOVA scores fluctuated as she went on and off carbamazepine, all four scales were normal months after she ceased taking carbamazepine. At that time, her TOVA performance showed no evidence of attentional deficit.

In a survey, 36 children, ages 6 years to 17 years, receiving EEG neurofeedback as a treatment for attention-deficit disorder (ADD)/ADHD were evaluated for changes in both subjective and objective clinical parameters (Alhambra et al., 1995). After 20 sessions, subjective improvement based on parental observations was 86%. In objective assessments, the overall improvement was 74% for TOVA score and 78% for favorable changes in QEEG parameters. Over a 12-month period, neurofeedback was associated with either a decrease or termination of pharmacotherapy in 16 of 24 patients receiving medication for ADD/ADHD.

In a retrospective study, 11 females, ages 12 years to 21 years, diagnosed with dissociative identity disorder (DID) received 30 neurofeedback and 10 group sessions (Manchester et al., 1998). The treatment was designed to increase prefrontal ß activity for alertness and simultaneously enhance activity associated with a reverie state. The combined increase of ß and brain waves allowed patients to re-experience their traumatic memories while in a hypnagogic reverie state but free of the distortions that arise during dreaming or hypnosis. The ratio of to ß activity is crucial in this type of training. If activity becomes too high, patients may sink into an unconscious state and not remember their past experiences. Three to 27 months following neurofeedback training, the post-treatment score for the DID group was 82, falling within the range of normal values. By bringing dissociated information, affect and sensation into consciousness, neurofeedback training helped subjects to resolve conflicts that contributed to their dissociative defense symptoms.

Neurofeedback resulted in favorable changes between pre- and post-treatment scores on the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) in a 65-year-old woman diagnosed with a major depressive disorder and in a 42-year-old woman with chronic psychological maladjustment (Baehr et al., 1997). The researchers concluded that even though EEG asymmetry training is not an efficacious stand-alone therapy for depression, it is an effective adjunct to psychotherapy for treating certain mood disorders.

Certain neurofeedback protocols may be beneficial for treating anxiety disorders (Moore, 2000), but the success of particular neurofeedback protocols for anxiety may depend on which diagnostic categories are used (Thomas and Sattlberger, 1997). Case studies on the effects of neurofeedback on bipolar disorder (BD) have produced mixed results. Although Rosenfeld (2000) was unsuccessful in treating two patients with BD using a neurofeedback protocol, Othmer (2001) found neurofeedback to be effective in managing mood swings in pediatric patients with BD when combined with pharmacotherapy and psychotherapy. In the Othmer case studies, neurofeedback protocols that directly affect inter-hemispheric communication were most efficacious for children diagnosed with BD.

In addition, EEG neurofeedback may have limited applicability for treating psychotic symptoms. Researchers successfully used neurofeedback to modulate slow potentials in schizophrenic and schizotypal subjects in the subacute phase (Gruzelier, 2000). And several studies show that neurofeedback is efficacious for long-term recovery in substance abusers (Kaiser et al., 1999; Trudeau, 2000).

Future Directions

Despite positive evidence from case studies, Russell A. Barkley, Ph.D., professor of psychiatry and neurology at University of Massachusetts Medical School, disputes claims that EEG neurofeedback has an effect on ADHD. Barkley told PT that EEG neurofeedback is not supported by evidence-based medicine. "One chief problem," he warned, "is that pre- and post-changes occur in subjects with ADHD regardless of whether or not they receive neurofeedback." Barkley attributed reported improvements in objective measures of ADHD symptoms (such as parent and teacher rating scales of disruptive behavior) to the practice effect. "Because of the lack of adequately designed studies, any effects associated with EEG neurofeedback may be due to the placebo response," Barkley said.

However, Lubar et al's. 1995 study provided comparative pre- and post-treatment measurements of several parameters in subjects with ADHD who improved and in those who did not. As noted, the pre-/post-changes observed in the neurofeedback-responsive treatment group were nearly equivalent to changes reported for pre-/post-medication in subjects with ADHD. Other studies comparing the effects of EEG neurofeedback and psychostimulants reveal that neurofeedback produces post-treatment changes equal to those associated with pharmacotherapy (Nash, 2000). Based on these findings, supporters argue that neurofeedback achieves its therapeutic effects by acting on electrophysiological substrates of the brain and not via a placebo response (Othmer et al., 1999).

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